Editorial: Host immune evasion by Mycobacterium tuberculosis: Current updates

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Host immune evasion by Mycobacterium tuberculosis: Current updatesMycobacterium tuberculosis (M.tb) can become a long-term infection by evading the host's immune response.Virulent mycobacterial strains employ various strategies to hijack the host's immune systems in favor of persistent infection and disease progression.Although the immune evasion mechanisms identified so far are already numerous, they most likely represent only the tip of the iceberg.Identifying fundamental pathogen virulence regulators and investigating the underlying immune mechanisms remain critical in the quest for more effective vaccines and therapeutic targets.Ubiquitin (Ub) targeting intracellular bacteria is a crucial innate immune mechanism in mammalian cells against intracellular pathogens.Herpesvirus-associated ubiquitinspecific protease (HAUSP USP7) is a deubiquitinase (DUB) that mediates the expression and function of proteins regulating cellular processes and modulating their state of ubiquitination (1, 2).Kim et al., 2022, now add this protease to the list of proteins exploited by M. tb to avoid host immune responses.M. tb possesses a unique family of proteins, named PE_PGRS.Recently, an increasing number of reports have shown that the mycobacterial PE_PGRS proteins play critical roles in bacterial pathogenesis and immune evasion (3).PE_PGRS38, encoded by Rv2162c in pathogenic mycobacterial species (4), is identified as a potential target for the second-line anti-TB drug, Capreomycin (5).Kim et al., 2022, found that PE_PGRS38 binds to HAUSP and thereby regulates the activity of various proteins through modulation of their state of ubiquitination.The overall downstream effect of PE_PGRS38 interaction with HAUSP increased intracellular survival of the bacteria and downregulated inflammatory cytokine levels.TNF Receptor Associated Factor 6 (TRAF6) is an intermediate protein in inflammatory-related signaling pathways and the regulation of its cytosolic level is crucial in maintaining cellular homeostasis (6-8).Mycobacterial antigens have been reported to interact with TRAF6 and thus regulate inflammation in the host.HAUSP is a Frontiers in Immunology frontiersin.

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